The study published inJournal of Clinical Endocrinology & Metabolism examines how T2D can cause the body to express a deficiency in metabolizing certain nutrients. By identifying these nutrients, the study brings attention to metabolic signatures that are present and develop into T2D.

People enrolled in the screening were divided into 3 groups, all were analyzed in the metabolic signaling of different nutrients The impaired fasting group (IFG) had HbA1c of less than 6.5%, the T2D group had HbA1c of greater than or equal to 6.5%,, and healthy controls had HbA1c of less than 6.1%.

Compared to healthy controls, those with IFG and T2D had significantly raised fructose and most other nutrients measured in the study. The IFG and T2D group also had significantly reduced pyroglutamic acid, glycerophospohlipids, and sphingomyelins.

The importance of these nutrients being significantly decreased has to do with what they do in nourishing the body. Pyroglutamic acid and glycerophospohlipids play a role in brain health and sphingomyelins enhances fat metabolism.

The most damaging metabolite changes observed were seen in the IFG and T2D groups. Abnormalities in their blood assays were seen in specific micronutrients such as amino acids, fatty acids, the membranes of most vegetables, fruits, grains, and animal cell membranes.

Your body has metabolic wiring. Impaired fasting glucose and T2D cause the normal metabolic signaling to be abnormally transmitted. If these conditions can weaken the metabolic signal, could there be a signal amplifier as treatment to correct this abnormality or would it just amplify the wrong message?